Hematology — MCQs

Hematology Indian Medical PG Practice Questions and MCQs

Question 1101: Thrombotic thrombocytopenic purpura is a syndrome characterized by which of the following?

A. Thrombocytopenia, anemia, neurological abnormalities, progressive renal failure and fever (Correct Answer)
B. Thrombocytopenia, anemia, neurological abnormalities, progressive hepatic failure and fever
C. Thrombocytopenia, normal anemia, neurological abnormalities, progressive renal failure and fever
D. Thrombocytopenia, anemia, no neurological abnormalities, progressive renal failure and fever

Explanation: ***Thrombocytopenia, anemia, neurological abnormalities, progressive renal failure and fever*** - Thrombotic thrombocytopenic purpura is characterized by **thrombocytopenia** and **microangiopathic hemolytic anemia**, along with neurological and renal complications [1][2]. - The presence of **fever** and other systemic symptoms is consistent with this **thrombotic microangiopathy** syndrome [1]. *Thrombocytosis, anemia, neurologic abnormalities, progressive renal failure and fever* - This option incorrectly lists **thrombocytosis** rather than **thrombocytopenia**, which is a hallmark of thrombotic thrombocytopenic purpura (TTP) [1]. - While it includes anemia, the absence of thrombocytopenia makes it inconsistent with TTP's classic presentation [2]. *Thrombocytopenia, anemia, neurologic abnormalities, progressive hepatic failure and fever* - Although it correctly states **thrombocytopenia** and **anemia**, it incorrectly identifies **progressive hepatic failure** instead of **renal failure**, which is a key feature of TTP [1]. - The presence of neurological abnormalities and fever does align with TTP; however, the hepatic failure aspect is misleading. *Thrombocytosis, anemia neurologic abnormalities, progressive renal failure and fever* - Again, this option incorrectly notes **thrombocytosis**, contradicting the characteristic finding of **thrombocytopenia** found in TTP [1]. - While other features align with TTP's clinical picture, the thrombocytosis excludes this option from being correct [2]. **References:** [1] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. The Kidney, pp. 947-948. [2] Kumar V, Abbas AK, et al.. Robbins and Cotran Pathologic Basis of Disease. 9th ed. Red Blood Cell and Bleeding Disorders, pp. 667-668.

Question 1102: Which of the following diseases is NOT associated with Anti-Neutrophil Cytoplasmic Antibodies (ANCA)?

A. Wegener's granulomatosis
B. Henoch schonlein purpura (Correct Answer)
C. Microscopic PAN
D. Churg Strauss syndrome

Explanation: ***Henoch schonlein purpura*** - **Henoch-Schönlein purpura (HSP)** is not associated with **ANCA**; it primarily involves IgA deposition [1]. - Commonly presents with **purpura**, **abdominal pain**, and **glomerulonephritis**, differentiating it from ANCA-associated vasculitides [1]. *Wegener's granulomatosis* - **Wegener's granulomatosis**, now known as **Granulomatosis with polyangiitis**, is strongly associated with **c-ANCA** and anti-PR3 antibodies. - It typically presents with **respiratory** and **renal symptoms** due to vasculitis [2]. *Microscopic PAN* - **Microscopic polyangiitis (PAN)** is associated with **p-ANCA** and myeloperoxidase (MPO) antibodies. - It leads to **glomerulonephritis** and **pulmonary hemorrhage**, indicating its vasculitic nature. *Churg Strauss syndrome* - **Churg-Strauss syndrome**, or **Eosinophilic Granulomatosis with Polyangiitis**, is associated with **p-ANCA** and perinuclear staining [1]. - Often presents with **asthma**, **eosinophilia**, and systemic vasculitis affecting multiple organs [1].

Question 1103: In a patient with suspected vitamin B12 deficiency, which condition would result in an abnormal Schilling test?

A. Amylase deficiency
B. Pancreatic endocrine insufficiency
C. Lipase deficiency
D. Intrinsic factor deficiency (Correct Answer)

Explanation: ***Intrinsic factor deficiency*** - The Schilling test assesses the absorption of **vitamin B12**. **Intrinsic factor** is crucial for B12 absorption in the ileum. - Deficiency of intrinsic factor, as seen in **pernicious anemia**, directly impairs B12 absorption, leading to an abnormal Schilling test result [1]. *Amylase deficiency* - **Amylase** is an enzyme involved in the digestion of carbohydrates, not vitamin B12 absorption [2]. - Its deficiency would primarily cause carbohydrate malabsorption symptoms, not an abnormal Schilling test. *Pancreatic endocrine insufficiency* - **Pancreatic endocrine function** relates to hormone production (e.g., insulin, glucagon), while exocrine function involves digestive enzymes. - Impairment of endocrine function does not directly affect vitamin B12 absorption or the Schilling test. *Lipase deficiency* - **Lipase** is an enzyme essential for the digestion of fats [2]. - Its deficiency would lead to fat malabsorption (steatorrhea) but would not affect vitamin B12 absorption or the Schilling test results.

Question 1104: Which of the following is not a recognized risk factor for deep vein thrombosis (DVT)?

A. Use of the oestrogen-progesterone contraceptive pills
B. Duration of surgery more than thirty minutes
C. Obesity
D. Age less than forty years (Correct Answer)

Explanation: The incidence of DVT increases with age, particularly after 40 years [1]. While DVT can occur at any age, it is much **less common in younger individuals** unless other significant risk factors are present [1]. *Duration of surgery more than thirty minutes* - **Prolonged immobility** during surgery, especially for durations longer than 30 minutes, significantly increases the risk of DVT due to venous stasis [2]. - Surgical procedures themselves can cause **endothelial injury** and activate the coagulation cascade, further contributing to thrombus formation [2]. *Obesity* - **Obesity** is a well-established risk factor for DVT, as it is associated with a hypercoagulable state and contributes to venous stasis due to increased intra-abdominal pressure and reduced mobility. - Adipose tissue also produces **pro-inflammatory cytokines** and other factors that promote thrombosis. *Use of the oestrogen-progesterone contraceptive pills* - **Combined oral contraceptive pills** containing oestrogen and progesterone are known to increase the risk of DVT by causing a hypercoagulable state. - Oestrogen can increase the levels of certain **clotting factors** (e.g., factors VII, VIII, X, and fibrinogen) and decrease levels of natural anticoagulants.

Question 1105: Which of the following conditions does not provide protection against malaria?

A. PNH (Correct Answer)
B. Sickle cell anemia
C. Thalassemia
D. Duffy blood group

Explanation: ***PNH*** - **Paroxysmal Nocturnal Hemoglobinuria (PNH)** does not provide protection against malaria; it is a disorder of the blood that leads to red blood cell destruction, but malaria specifically targets red blood cells. - PNH is associated with increased risk of venous thrombosis and hemolytic anemia, rather than any protective mechanism against malaria. *Sickle cell anemia* - The sickle cell trait provides a **protective advantage** against malaria by offering some resistance due to the abnormal shape of the cells [1]. - Individuals with the trait have a lower risk of severe malaria, particularly caused by *Plasmodium falciparum* [1]. *Duffy blood group* - People with the **Duffy negative phenotype** are resistant to certain strains of malaria, as the Duffy antigen serves as a receptor for *Plasmodium vivax*. - Therefore, those lacking the Duffy antigen are less susceptible to infections by this malaria strain. *Thalassemia* - Thalassemia provides a protective effect against malaria by producing **abnormal hemoglobin**, which malaria parasites cannot easily thrive in [2]. - This leads to an altered red blood cell environment that is less favorable for *Plasmodium* infection [1].

Question 1106: Which of the following conditions is the classic example of acute intravascular hemolysis triggered by oxidative stress?

A. Hereditary spherocytosis
B. Sickle cell disease
C. Acute G6PD deficiency (Correct Answer)
D. None of the options

Explanation: ***b and c*** - Intravascular hemolysis is commonly associated with both **Acute G6PD deficiency** and **Hereditary spherocytosis**, leading to destruction of red blood cells in the bloodstream [1]. - These conditions are characterized by **high levels of hemoglobinuria** and **low haptoglobin**, indicative of intravascular hemolysis. *Sickle cell ds* - Sickle cell disease primarily causes **extravascular hemolysis** due to splenic sequestration rather than **intravascular** destruction [3]. - The clinical features include **vaso-occlusive crises** and splenic infarction rather than hemolysis within the blood vessels. *Acute G6PD* - While acute G6PD deficiency can lead to hemolysis, it is typically **triggered by oxidative stress** rather than occurring continuously [2]. - The hemolysis in G6PD deficiency occurs more in an **extravascular** manner unless acute stress occurs, which can result in **acute intravascular hemolysis, marked by anemia, hemoglobinemia, and hemoglobinuria** [4]. *Hereditary spherocytosis* - This condition primarily causes **extravascular hemolysis** through the spleen, where abnormal spherocytes are destroyed [1]. - Although it leads to anemia, the hallmark of hereditary spherocytosis is the **spleen's role** in hemocyte destruction rather than intravascular hemolysis.

Question 1107: PNH patients have deficient surface proteins that normally protect red blood cells from activated complements. Which two surface proteins are deficient in these patients?

A. CD 55 and CD 58
B. CD 45 and CD 55 (Correct Answer)
C. CD 55 and CD 59
D. CD 51 and CD 55

Explanation: ***CD 55 and CD 59*** - **CD 55 (decay accelerating factor)** and **CD 59 (protectin)** are crucial for inhibiting the complement system, protecting red blood cells from lysis in PNH. - Deficiencies in these proteins lead to increased **susceptibility** of red cells to **complement-mediated hemolysis**. *CD58 and CD 59* - **CD 58** is involved in T-cell interaction but does not solely protect red cells from complement. - While **CD 59** is a correct answer, the absence of **CD 55** makes this option incorrect for PNH. *CD 45 and CD 59* - **CD 45** is primarily a **leukocyte common antigen**, not involved in protecting red cells from complement activation. - This orrectly mentions **CD 59**, but lacks **CD 55**, making it unsuitable as an answer. *CD 51 and CD 59* - **CD 51** is associated with integrin functions and does not play a role in protecting red blood cells from complements. - Although **CD 59** is relevant, the deficiency in **CD 55** highlights the incompleteness of this option.

Question 1108: In which condition is venous blood most commonly observed to have a high hematocrit in routine clinical practice?

A. Dehydration (Correct Answer)
B. Anemia
C. Hypervolemia
D. Acute blood loss

Explanation: Dehydration - In **dehydration**, the total body water is reduced, leading to a decrease in plasma volume [1, 5]. This concentrates the red blood cells, resulting in a relatively **high hematocrit**. [3] - This is a common finding as the body attempts to conserve fluid, making it a primary cause of **elevated hematocrit** in clinical practice. *Anemia* - **Anemia** is characterized by a decrease in the number of red blood cells or a reduced hemoglobin concentration, which would lead to a **low hematocrit**, not a high one [2]. - This condition involves insufficient oxygen-carrying capacity due to a deficiency in red blood cells or hemoglobin [2]. *Hypervolemia* - **Hypervolemia** describes an excess of fluid in the blood, which would dilute the blood components, leading to a relatively **low hematocrit** [1]. - This condition is often associated with conditions like heart failure or kidney disease, where fluid retention is common. *Acute blood loss* - In **acute blood loss**, the loss of whole blood immediately after the event would initially reduce both red blood cells and plasma proportionally, not immediately raising hematocrit [2]. - As the body attempts to compensate by shifting extravascular fluid into the circulation, this would further dilute the blood, eventually leading to a **decreased hematocrit** [2].

Question 1109: Which condition is commonly associated with Disseminated Intravascular Coagulation (D.I.C.)?

A. Acute myelomonocytic leukemia
B. Chronic myeloid leukemia
C. Autoimmune hemolytic anemia
D. Acute promyelocytic leukemia (Correct Answer)

Explanation: ***Acute promyelocytic leukemia*** - **Disseminated Intravascular Coagulation (D.I.C.)** is commonly associated with acute promyelocytic leukemia due to the release of **tissue factor** from promyelocytes [1]. - Patients typically present with **severe bleeding** and coagulopathy [1], driven by the rapid proliferation of these abnormal cells. *Acute myelomonocytic leukemia* - While this type of leukemia presents with myelomonocytic features, it is less frequently associated with **D.I.C.** compared to acute promyelocytic leukemia. - This condition is often characterized by **monocytic infiltration** but does not typically cause the severe coagulopathy associated with D.I.C. *Autoimmune hemolytic anemia* - This condition causes **hemolysis** due to antibodies but is mainly associated with **anemia**, not a coagulation disorder like D.I.C. - **D.I.C.** involves widespread **consumption coagulopathy** [1], which is not a feature of autoimmune hemolytic anemia. *CMC* - CMC refers to **Chronic Myeloid Leukemia**, which does not commonly lead to **D.I.C.** and presents primarily with splenomegaly and **chronic symptoms**. - The coagulation profile in CMC tends to be stable, with no link to the acute coagulopathy seen in D.I.C.

Question 1110: Which of the following statements regarding iron supplementation in iron deficiency anemia is incorrect?

A. Administer a small diluted dose first prior to infusion to look for any allergy to iron preparation
B. If gastric intolerance to oral iron therapy occurs, all patients should be administered parenteral forms (Correct Answer)
C. Parenteral iron supplementation is required in a patient with Hb of less than 7 mg/dL
D. Oral iron therapy should be stopped once the patient achieves a hemoglobin of >12 mg/dL

Explanation: ### *If gastric intolerance to oral iron therapy occurs, all patients should be administered parenteral forms* - Not all patients experiencing gastric intolerance to oral iron therapy **require immediate parenteral iron**. Strategies like switching to a different oral iron formulation, taking iron with food, or using a **lower dose** can often alleviate symptoms. - Parenteral iron is typically reserved for cases where oral iron is truly ineffective, poorly tolerated despite modifications, or when rapid iron repletion is critically needed, such as in severe **anemia or ongoing blood loss**. ### *Administer a small diluted dose first prior to infusion to look for any allergy to iron preparation* - Administering a small, diluted test dose of **intravenous iron** is a common and recommended practice before a full infusion to assess for immediate allergic reactions. - This precautionary step helps to identify patients who may experience **hypersensitivity reactions**, ranging from mild to severe **anaphylaxis**, to the iron preparation. ### *Parenteral iron supplementation is required in a patient with Hb of less than 7 mg/dL* - A hemoglobin (Hb) level of less than 7 mg/dL indicates **severe anemia**, which often warrants rapid iron repletion. - While parenteral iron is frequently used in such severe cases, particularly if there's ongoing blood loss or malabsorption, it is not an absolute requirement; **oral iron** can still be effective if tolerated and sufficient time is available for absorption. ### *Oral iron therapy should be stopped once the patient achieves a hemoglobin of >12 mg/dL* - Oral iron therapy should not be stopped immediately once hemoglobin levels normalize (e.g., >12 mg/dL) [1]. - It is crucial to continue iron supplementation for several months after hemoglobin normalization [2] to replenish **iron stores** (ferritin levels) [1].

Practice by Chapter

Anemia Evaluation and Management

Practice Questions

Hemoglobinopathies

Practice Questions

Thalassemias

Practice Questions

Platelet Disorders

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Coagulation Disorders

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Thrombotic Disorders

Practice Questions

Leukemias

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Lymphomas

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Multiple Myeloma and Plasma Cell Disorders

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Myeloproliferative Neoplasms

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Transfusion Medicine

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Hematopoietic Stem Cell Transplantation

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Hematology — MCQs

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